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      CELL PROLIFERATION AND CYTOKINE INDUCTION BY TNF-α OF PSORIATIC KERATINOCYTES ARE NOT DIFFERENT FROM NORMAL KERATINOCYTES IN VITRO

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          Abstract

          Background:

          Recent studies indicate that various cytokines including tumor necrosis factor-α (TNF-α) play an essential role in the induction and maintenance of psoriatic lesion.

          Aims:

          To compare the cell proliferation of keratinocytes by various cytokines and TNF-α-induced cytokine secretion among normal keratinocytes, uninvolved, and involved keratinocytes.

          Methods:

          The keratinocytes from normal skin, uninvolved, and involved psoriasis were cultured in the presence of IL-6, IL-8, epidermal growth factor (EGF), hepatocyte growth factor (HGF), transforming growth factor-α (TGF-α) epiregulin, amphiregulin, and TNF-α and then MTT assay for keratinocytes proliferation was performed. Furthermore, TNF-α-induced secretion of IL-6, IL-8, EGF, HGF, TGF-α, epiregulin, and amphiregulin were compared among these keratinocytes.

          Results:

          IL-6, IL-8, EFG, TGF-α, epiregulin, and amphiregulin, but not TNF-α increased keratinocyte proliferation of normal, psoriatic uninvolved, and involved skin. The increased cell proliferation by these cytokines and growth factors were not different among the keratinocytes derived from normal skin, uninvolved, and involved psoriasis. The significant induction of TNF-α increased IL-6, IL-8, EGF, HGF, TGF-α, epiregulin, and amphiregulin, but the increase in these cytokines and growth factors were not different among normal skin, uninvolved, and involved psoriasis.

          Conclusion:

          Cell proliferation by various cytokines and growth factors and TNF-α-induced cytokine secretion are not different between normal and psoriatic keratinocytes.

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          Most cited references11

          • Record: found
          • Abstract: found
          • Article: not found

          Pathogenesis and therapy of psoriasis.

          Psoriasis is one of the most common human skin diseases and is considered to have key genetic underpinnings. It is characterized by excessive growth and aberrant differentiation of keratinocytes, but is fully reversible with appropriate therapy. The trigger of the keratinocyte response is thought to be activation of the cellular immune system, with T cells, dendritic cells and various immune-related cytokines and chemokines implicated in pathogenesis. The newest therapies for psoriasis target its immune components and may predict potential treatments for other inflammatory human diseases.
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            • Record: found
            • Abstract: found
            • Article: not found

            Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses

            Biological agents have dramatically improved treatment options for patients with severe psoriasis. Etanercept (tumor necrosis factor [TNF] receptor–immunoglobulin fusion protein) is an effective treatment for many psoriasis patients, and blockade of TNF is considered to be its primary action. However, in this clinical trial, we show that etanercept has early inhibitory effects on a newly appreciated type of T cells: T helper type 17 (Th17) cells. Etanercept reduced the inflammatory dendritic cell products that drive Th17 cell proliferation (interleukin [IL] 23), as well as Th17 cell products and downstream effector molecules (IL-17, IL-22, CC chemokine ligand 20, and β-defensin 4). In contrast, Th1 cellular products and effector molecules (interferon γ, lymphotoxin α, and myxovirus resistance 1) were reduced late in disease resolution. This study suggests a role for Th17 in addition to Th1 cells in the pathogenesis of psoriasis. Th17 cells may be particularly important in driving epidermal activation in psoriatic plaques, whereas Th1 cells must also be eliminated for final disease resolution.
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              • Record: found
              • Abstract: not found
              • Article: not found

              Cracking the cytokine code in psoriasis.

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                Author and article information

                Journal
                Indian J Dermatol
                IJD
                Indian Journal of Dermatology
                Medknow Publications (India )
                0019-5154
                1998-3611
                Jul-Sep 2009
                : 54
                : 3
                : 237-239
                Affiliations
                From the Department of Dermatology, Asahikawa Medical College, 2-1-1-1 Midorigaokahigashi, Asahikawa 078-8510, Japan.
                Author notes
                Address for correspondence: Dr. Hidetoshi Takahashi, Department of Dermatology, Asahikawa Medical College, 2-1-1-1 Midorigaokahigashi, Asahikawa 078-8510, Japan. E-mail: ht@ 123456asahikawa-med.ac.jp
                Article
                IJD-54-237
                10.4103/0019-5154.55631
                2810688
                20161853
                e9ba1a10-0b1a-46c9-a9be-3a38c8fdb046
                © Indian Journal of Dermatology

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : March 2009
                : March 2009
                Categories
                Basic Research

                Dermatology
                tnf-α,psoriasis,cell proliferation
                Dermatology
                tnf-α, psoriasis, cell proliferation

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